Genistein Prevents Prostate Cancer Metastasis In Animal Model

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March 14, 2008

Genistein prevents prostate cancer metastasis in animal model

Genistein prevents prostate cancer metastasis in animal model

The March 15, 2008 issue of the journal Cancer Research published the finding of a team from Northwestern University in Illinois that genistein, an antioxidant compound that occurs in soybeans, almost completely prevented prostate cancer from spreading in mice in whom cancerous human tissue was implanted. The study is the first to show that genistein can halt prostate cancer metastasis in a living organism.

Raymond C. Bergan, MD of Northwestern’s Robert H. Lurie Comprehensive Cancer Center and his colleagues implanted an aggressive human form of prostate cancer into several groups of mice and gave some of the animals an amount of genistein that elevated blood concentrations to levels comparable to those measured in humans following the consumption of soy foods. While genistein did not reduce prostate tumor size, spread of the disease to the lungs, a common site of metastasis, was reduced by 96 percent compared with animals that did not receive genistein. A repeat of the experiment elicited the same result.

In previous research conducted by Dr Bergan’s team using prostate cancer cell cultures, it was discovered that genistein prevents the detachment of cancer cells from a primary tumor and blocks cell invasion. This is accomplished by the inhibition of the activation of molecules called p38 MAP kinases which are involved in the activation of proteins that loosen cancerous cells from tumors and cause them to migrate. “In culture, you can actually see that when genistein is introduced, cells flatten themselves in order to spread out and stick strongly to nearby cells,” Dr Bergan commented.

Surprisingly, the current investigation found that animals that received genistein had higher levels of expression of genes involved in cancer cell migration. “What we think is happening here is that the cells we put in the mice normally like to move,” Dr Bergan explained. “When genistein restricted their ability to do so, they tried to compensate by producing more protein involved in migration. But genistein prevented those proteins from being activated. This is really a lesson for researchers who depend on biomarker studies to test whether a treatment is working. They need to be aware that those biomarkers might be telling only half of the story.”

“These impressive results give us hope that genistein might show some effect in preventing the spread of prostate cancer in patients,” Dr Bergan concluded. “Diet can affect cancer and it doesn’t do it by magic. Certain chemicals have beneficial effects and now we have all the preclinical studies we need to suggest genistein might be a very promising chemopreventive drug.”

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Health Concern Life Extension Highlight

Prostate cancer

Every cancer, including prostate cancer, is a disordered and abnormal cell growth. Cancer cells have lost the ability to network and communicate in the way that normal cells do, and they no longer function as intended in the overall framework of body chemistry. Such cells take on a demeanor of juvenile delinquents, with no respect for parental direction. Attempts to restrict disruptive or nonproductive behavior are ignored. Such disruptive cells are usually censored and expelled by regulatory monitors--guardians of the genome, proteins such as p53, p21, and p27, which normally identify and biologically excise such maladapted cells. In malignant conditions, these regulatory proteins lose control for largely unknown reasons.

In one study involving the development of malignancy of the esophagus, antibodies to p53 were found in 4 of 36 (11%) premalignant lesions of the esophagus and in 10 of 33 (30%) of those with cancer of the esophagus. In two of the esophageal cancer patients, the p53 antibodies were detected prior to a clinical diagnosis of cancer. Therefore, the cellular counterparts of terrorists are finding a way past one of the surveillance mechanisms (p53) that usually stand guard to detect DNA damage and halt the machinery of the cell cycle in G1 or G2 when DNA defects are found.

The development of malignancy results from a combination of hits on the cell--repeated insults. Ongoing promotional and progression events eventually lead to premalignant changes such as prostatic intraepithelial neoplasia (PIN), then to noninvasive cancer, and finally to invasive cancer. If not diagnosed early and eradicated, metastatic cancer may eventually develop.

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